Inhibition of Fatty Acid Translocase (FAT/CD36) Palmitoylation Enhances Hepatic Fatty Acid β-Oxidation by Increasing Its Localization to Mitochondria and Interaction with Long-Chain Acyl-CoA Synthetase 1

CD36 棕榈酰化 线粒体 脂肪酸 生物化学 生物 肝细胞 β氧化 化学 基因 体外 半胱氨酸
作者
Shu Zeng,Fan Wu,Mengyue Chen,Yun Li,Mengyue You,Yang Zhang,Ping Yang,Wei Li,Xiong Z. Ruan,Lei Zhao,Yaxi Chen
出处
期刊:Antioxidants & Redox Signaling [Mary Ann Liebert, Inc.]
卷期号:36 (16-18): 1081-1100 被引量:72
标识
DOI:10.1089/ars.2021.0157
摘要

Aims: Impaired fatty acid oxidation (FAO) in mitochondria of hepatocytes causes lipid accumulation and excessive production of reactive oxygen species (ROS) and oxidative damage, leading to nonalcoholic fatty liver disease (NAFLD). Fatty acid translocase (FAT/cluster of differentiation 36 [CD36]), a transmembrane protein that facilitates the uptake of long-chain fatty acids (LCFAs), is recently found to be involved in FAO. The function of FAT/CD36 is associated with its subcellular localization. Palmitoylation, one of the most common lipid modifications, is generally thought to regulate FAT/CD36 subcellular localization. Here, we aimed to investigate the role of palmitoylation in FAT/CD36 localization to mitochondria and its influence on FAO in hepatocytes. Results: We demonstrated that FAT/CD36 exists on the mitochondria of hepatocytes. Palmitoylation of FAT/CD36 was significantly upregulated in NAFLD. Inhibition of FAT/CD36 palmitoylation resulted in an obvious increase in the distribution of FAT/CD36 to mitochondria of hepatocytes. Depalmitoylated FAT/CD36 on the mitochondrial membrane continues functioning by facilitating fatty acid trafficking to mitochondria. Abundant mitochondrial FAT/CD36 interacted with long-chain acyl-CoA synthetase 1 (ACSL1), and thus, more LCFAs were transported to ACSL1. This led to an increase in the generation of long-chain acyl-CoA, contributing to the enhancement of FAO and alleviating NAFLD. Innovation and Conclusion: This work revealed that inhibiting FAT/CD36 palmitoylation alleviates NAFLD by promoting FAT/CD36 localization to the mitochondria of hepatocytes. Mitochondrial FAT/CD36 functions as a molecular bridge between LCFAs and ACSL1 to increase the production of long-chain acyl-CoA, thus promoting FAO, thereby avoiding lipid accumulation and overproduction of ROS in hepatocytes. Antioxid. Redox Signal. 36, 1081–1100.
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